CD1d deficiency exacerbates inflammatory dermatitis in MRL-lpr/lpr mice.

Yang JQ, Chun T, Liu H, Hong S, Bui H, Van Kaer L, Wang CR, Singh RR
Eur J Immunol. 2004 34 (6): 1723-32

PMID: 15162443 · PMCID: PMC2291526 · DOI:10.1002/eji.200324099

Mechanisms responsible for the development of autoimmune skin disease in humans and animal models with lupus remain poorly understood. In this study, we have investigated the role of CD1d, an antigen-presenting molecule known to activate natural killer T cells, in the development of inflammatory dermatitis in lupus-susceptible MRL-lpr/lpr mice. In particular, we have established MRL-lpr/lpr mice carrying a germ-line deletion of the CD1d genes. We demonstrate that CD1d-deficient MRL-lpr/lpr mice, as compared with wild-type littermates, have more frequent and more severe skin disease, with increased local infiltration with mast cells, lymphocytes and dendritic cells, including Langerhans cells. CD1d-deficient MRL-lpr/lpr mice had increased prevalence of CD4(+) T cells in the spleen and liver and of TCR alpha beta (+)B220(+) cells in lymph nodes. Furthermore, CD1d deficiency was associated with decreased T cell production of type 2 cytokines and increased or unchanged type 1 cytokines. These findings indicate a regulatory role of CD1d in inflammatory dermatitis. Understanding the mechanisms by which CD1d deficiency results in splenic T cell expansion and cytokine alterations, with increased dermal infiltration of dendritic cells and lymphocytes in MRL-lpr/lpr mice, will have implications for the pathogenesis of inflammatory skin diseases.

MeSH Terms (20)

Animals Antigens, CD1 Antigens, CD1d CD4-Positive T-Lymphocytes Dermatitis Disease Models, Animal Female Immunohistochemistry Immunophenotyping Interferon-gamma Interleukin-4 Interleukin-10 Liver Male Mice Mice, Inbred MRL lpr Mice, Knockout Nephritis Organ Size Thymus Gland

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